Possible Trimethoprim–Sulfamethoxazole-Induced Hemolytic Anemia: A Case Report

Williams, Montgomery F; Doss, Emily P; Montgomery, Maggie

doi:10.1177/0897190016683303

Cited by 5 publications

(3 citation statements)

References 6 publications

(35 reference statements)

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“…Antibiotics including penicillin and cephalosporins are the drugs most often implicated in the development of AIHA (12). Autoimmune hemolytic anemia associated with other classes of antibiotics such as trimethoprim sulfamethoxazole has also been reported in few cases in literature (13,14).…”

Section: Discussionmentioning

confidence: 99%

Autosomal Recessive Polycystic Kidney Disease in a Child Complicated by Autoimmune Hemolytic Anemia: A Case Report

Kotb

Baky²,

Sayed³

et al. 2023

Pediatric Sciences Journal

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Autosomal recessive polycystic kidney disease (ARPKD) is a rare genetic disorder that presents as an isolated polycystic renal disease in childhood, or associated with congenital hepatic fibrosis and/or Caroli disease. The spectrum of complications of ARPKD include end stage kidney disease, systemic hypertension and liver disease. Anemia in ARPKD is commonly due to be reduced erythropoietin or iron deficiency. We present a 2-year old male patient with ARPKD who presented to the emergency room by striking pallor and dark urine. Initial lab work revealed Hemoglobin level 2g/dL. Blood transfusion was challenging due to difficult typing and frequent mismatch. Other labs showed elevated urea and creatinine, positive direct Coomb's anticoagulant test and positive urine culture. Imaging was consistent with ARPKD. The patient was resuscitated and after stabilization, he received pulsed methylprednisolone at 30 mg/day for 5 days followed by prednisone 2mg/kg/day for 4 weeks that was tapered over 2 months with marked improvement. Herein we report autoimmune hemolytic anemia as another and rare cause for anemia associated with ARPKD.

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Section: Discussionmentioning

confidence: 99%

Autosomal Recessive Polycystic Kidney Disease in a Child Complicated by Autoimmune Hemolytic Anemia: A Case Report

Kotb

Baky²,

Sayed³

et al. 2023

Pediatric Sciences Journal

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“…Supporting this notion, use of TMP is counter indicated in patients with folate deficiencies due to the rare possibility of anemia-related complications after high doses of TMP (and sulfamethoxazole). 59 – 61 Yet, these folate-related issues can likely be remedied simply by additional folate intake either through vitamins or dietary means.…”

Section: Discussionmentioning

confidence: 99%

A Destabilizing Domain Allows for Fast, Noninvasive, Conditional Control of Protein Abundance in the Mouse Eye – Implications for Ocular Gene Therapy

Datta

Renwick

Chau

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PurposeTemporal and reversible control of protein expression in vivo is a central goal for many gene therapies, especially for strategies involving proteins that are detrimental to physiology if constitutively expressed. Accordingly, we explored whether protein abundance in the mouse retina could be effectively controlled using a destabilizing Escherichia coli dihydrofolate reductase (DHFR) domain whose stability is dependent on the small molecule, trimethoprim (TMP).MethodsWe intravitreally injected wild-type C57BL6/J mice with an adeno-associated vector (rAAV2/2[MAX]) constitutively expressing separate fluorescent reporters: DHFR fused to yellow fluorescent protein (DHFR.YFP) and mCherry. TMP or vehicle was administered to mice via oral gavage, drinking water, or eye drops. Ocular TMP levels post treatment were quantified by LC-MS/MS. Protein abundance was measured by fundus fluorescence imaging and western blotting. Visual acuity, response to light stimulus, retinal structure, and gene expression were evaluated after long-term (3 months) TMP treatment.ResultsWithout TMP, DHFR.YFP was efficiently degraded in the retina. TMP achieved ocular concentrations of ∼13.6 μM (oral gavage), ∼331 nM (drinking water), and ∼636 nM (eye drops). Oral gavage and TMP eye drops stabilized DHFR.YFP as quickly as 6 hours, whereas continuous TMP drinking water could stabilize DHFR.YFP for ≥3 months. Stabilization was completely and repeatedly reversible following removal/addition of TMP in all regimens. Long-term TMP treatment had no impact on retina function/structure and had no effect on >99.9% of tested genes.ConclusionsThis DHFR-based conditional system is a rapid, efficient, and reversible tool to effectively control protein expression in the retina.

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“…Nevertheless, the application of this finding to clinical practice is limited and should not prevent clinicians from utilizing these medications for its more important renoprotective/ cardioprotective effects [12]. Other medications commonly used in kidney transplant patients that may cause anaemia include ganciclovir, valganciclovir and trimethoprim-sulfamethoxazole [26][27][28][29].…”

Section: Other Medicationsmentioning

confidence: 99%

The current therapeutic approach for anaemia after kidney transplant

Nissaisorakarn

Kantachuvesiri

2022

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of reviewAnaemia after kidney transplantation is a common finding with no uniform management guideline. Most approaches are derived from the chronic kidney disease (CKD) population. Recent advances for the treatment of anaemia in patients with CKD/End stage renal disease include hypoxia-inducible factor-prolyl hydroxylase inhibitor (HIF-PHi), a novel class of oral erythropoietin-stimulating agents (ESAs). We present relevant studies of HIF-PHi in the transplant population and its implications on the management of posttransplant anaemia.Recent findingsData on HIF-PHi use in the kidney transplant population are promising. Limited data demonstrate a significant increase in haemoglobin, with a comparable safety profile to epoetin. Reported adverse effects include overcorrection and low iron stores.SummaryCurrent therapeutic approaches to anaemia in the kidney transplant population is mostly derived from the CKD population. More studies are needed on HIF-Phi, a novel class of ESAs that has thus far demonstrated promise in the kidney transplant population.

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Possible Trimethoprim–Sulfamethoxazole-Induced Hemolytic Anemia: A Case Report

Abstract: We report a case of hemolytic anemia resulting from the use of TMP-SMX. Although this is a rare adverse effect, clinicians should be aware of the signs and symptoms of hemolytic anemia, and so appropriate treatment can be administered should it occur.

Cited by 5 publications

References 6 publications

Autosomal Recessive Polycystic Kidney Disease in a Child Complicated by Autoimmune Hemolytic Anemia: A Case Report

Autosomal Recessive Polycystic Kidney Disease in a Child Complicated by Autoimmune Hemolytic Anemia: A Case Report

A Destabilizing Domain Allows for Fast, Noninvasive, Conditional Control of Protein Abundance in the Mouse Eye – Implications for Ocular Gene Therapy

The current therapeutic approach for anaemia after kidney transplant

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